Using the yeast Saccharomyces cerevisiae we are examining mitotically identified DNA repair systems during normal meiosis. Several mutants in the UV and X-ray repair pathways are being used: radl (excision), rad52 (X-ray) and rad6 (mutational). The initiation of meiotic DNA synthesis is normal in the mutants and excision repair mutants are like wild-type for the other aspects of meiosis: recombination, haploidization, and size of DNA. In rad6, rad52 and rad50 mutants, recombination is abolished and for rad52 and rad50 the spore products are inviable. The rad52 mutant accumulates single-strand interruptions (SSI's) with the onset of premeiotic DNA synthesis and their occurrence coincides with commitment to cell death. Based on an absence of SSI's in a rad50 mutant and corresponding genetic observations, the RAD50 gene product precedes RAD52 in the molecular processing of DNA during meiosis. The RAD50 gene product may enable breaks or gaps to occur and the RAD52 gene product, which controls a single-strand deoxyribonuclease may process these gaps. In the absence of correct processing, the interrupted meiotic events lead to cell death.